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1. Huh JY, Chung S, Oh D, Kang MS, Eom HS, Cho EH, Han MH, Kong SY: Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature. Korean J Lab Med; 2010 Apr;30(2):117-21
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  • [Title] Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.
  • The translocation t(10;11)(p13;q14q21) has been found to be recurrent in acute lymphoblastic and myeloid leukemias, and results in the fusion of the clathrin assembly lymphoid myeloid leukemia (CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.
  • Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for acute leukemia.
  • The first patient (case 1) was diagnosed with T-cell ALL, and the second patient (case 2) was diagnosed with AML.
  • Both patient samples showed expression of the homeobox A gene cluster and the histone methyltransferase hDOT1L, which suggests that they mediate leukemic transformation in CALM-AF10-positive and mixed-lineage leukemia-AF10-positive leukemias.
  • Both patients achieved complete remission after induction chemotherapy.
  • The first patient (case 1) relapsed after double-unit cord blood transplantation; there was no evidence of relapse in the second patient (case 2) after allogenic peripheral blood stem cell transplantation.
  • Since CALM-AF10- positive leukemias have been shown to have poor prognosis with conventional therapy, molecular tests for CALM-AF10 rearrangement would be necessary to detect minimal residual disease during follow-up.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Monomeric Clathrin Assembly Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow / pathology. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Cord Blood Stem Cell Transplantation. Female. Histone-Lysine N-Methyltransferase / genetics. Histone-Lysine N-Methyltransferase / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Recurrence. Translocation, Genetic

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  • (PMID = 20445327.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 14
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2. Gong H, Liu WL, Zhou JF, Xu HZ: [Expression of mitosis checkpoint gene CHFR in acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1085-8
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  • [Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].
  • OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.
  • METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
  • The cell cycle was examined by flow cytometric analysis.
  • (1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
  • CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.
  • Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16029562.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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3. Rutar T, Cockerham KP: Periorbital zygomycosis (mucormycosis) treated with posaconazole. Am J Ophthalmol; 2006 Jul;142(1):187-188
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  • PURPOSE: To report on the successful treatment of periorbital zygomycosis (mucormycosis) with posaconazole, a broad-spectrum oral antifungal available for compassionate use.
  • RESULTS: A 22-year-old male undergoing induction chemotherapy for acute lymphoblastic leukemia presented with periorbital cellulitis attributable to Rhizopus.
  • He took posaconazole for five months while undergoing additional cycles of chemotherapy.
  • Despite recurrent profound neutropenia, the periorbital infection resolved, he tolerated reconstructive procedures, and he did not develop orbital invasion.
  • CONCLUSIONS: Drug toxicities can limit the use of amphotericin in some patients with zygomycosis.
  • Posaconazole shows promise as an alternative antifungal agent in the treatment of periorbital zygomycosis.
  • [MeSH-major] Antifungal Agents / therapeutic use. Eye Infections, Fungal / drug therapy. Mucormycosis / drug therapy. Orbital Diseases / drug therapy. Rhizopus / isolation & purification. Triazoles / therapeutic use
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Humans. Male. Microbial Sensitivity Tests. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Tomography, X-Ray Computed

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  • (PMID = 16815283.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Triazoles; 6TK1G07BHZ / posaconazole
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4. Hijiya N, Ness KK, Ribeiro RC, Hudson MM: Acute leukemia as a secondary malignancy in children and adolescents: current findings and issues. Cancer; 2009 Jan 1;115(1):23-35
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  • [Title] Acute leukemia as a secondary malignancy in children and adolescents: current findings and issues.
  • Secondary acute leukemia is a devastating complication in children and adolescents who have been treated for cancer.
  • Secondary acute lymphoblastic leukemia (s-ALL) was rarely reported previously but can be distinguished today from recurrent primary ALL by comparison of immunoglobulin and T-cell receptor rearrangement.
  • Secondary acute myeloid leukemia (s-AML) is much more common, and some cases actually may be second primary cancers.
  • Treatment-related and host-related characteristics and their interactions have been identified as risk factors for s-AML.
  • The most widely recognized treatment-related risk factors are alkylating agents and topoisomerase II inhibitors (epipodophyllotoxins and anthracyclines).
  • The magnitude of the risk associated with these factors depends on several variables, including the administration schedule, concomitant medications, and host factors.
  • The prevalence of alkylator-associated s-AML has diminished among pediatric oncology patients with the reduction of cumulative alkylator dose and limited use of the more leukemogenic alkylators.
  • The best-documented topoisomerase II inhibitor-associated s-AML is s-AML associated with epipodophyllotoxins.
  • The risk of s-AML in these cases is influenced by the schedule of drug administration and by interaction with other antineoplastic agents but is not consistently found to be related to cumulative dose.
  • The unpredictable risk of s-AML after epipodophyllotoxin therapy may discourage the use of these agents, even in patients at a high risk of disease recurrence, although the benefit of recurrence prevention may outweigh the risk of s-AML.
  • Studies in survivors of adult cancers suggest that, contrary to previous beliefs, the outcome of s-AML is not necessarily worse than that of de novo AML when adjusted for cytogenetic features.

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  • [Copyright] Copyright (c) 2008 American Cancer Society.
  • [Cites] Lancet. 1996 Feb 3;347(8997):295-7 [8569364.001]
  • [Cites] N Engl J Med. 1996 Mar 21;334(12):745-51 [8592547.001]
  • [Cites] J Natl Cancer Inst. 1996 Dec 18;88(24):1840-7 [8961974.001]
  • [Cites] Cancer. 1997 Mar 1;79(5):1049-54 [9041170.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2247-53 [9196137.001]
  • [Cites] Leukemia. 1998 Mar;12(3):346-52 [9529129.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3617-23 [10339466.001]
  • [Cites] Blood. 1999 Jul 15;94(2):803-7 [10397748.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3221-5 [10506622.001]
  • [Cites] Bone Marrow Transplant. 1999 Oct;24(7):735-9 [10516676.001]
  • [Cites] J Clin Oncol. 2004 Dec 15;22(24):4926-33 [15611507.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):926-7 [15681547.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Leukemia. 2006 Feb;20(2):239-46 [16341039.001]
  • [Cites] Oncogene. 2006 Sep 25;25(43):5875-84 [16998502.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Nov;15(11):2020-6 [17057028.001]
  • [Cites] Blood. 2007 Jan 1;109(1):46-51 [16985182.001]
  • [Cites] Bone Marrow Transplant. 2007 Jan;39(2):59-70 [17143301.001]
  • [Cites] J Clin Oncol. 2007 Jan 20;25(3):292-300 [17159192.001]
  • [Cites] J Natl Cancer Inst. 2007 Feb 7;99(3):196-205 [17284714.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):493-500 [17290056.001]
  • [Cites] Best Pract Res Clin Haematol. 2007 Mar;20(1):29-37 [17336252.001]
  • [Cites] JAMA. 2007 Mar 21;297(11):1207-15 [17374815.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1431-5 [17460701.001]
  • [Cites] Ophthalmology. 2007 Jul;114(7):1378-83 [17613328.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1379-87 [17488876.001]
  • [Cites] J Clin Oncol. 2007 Sep 1;25(25):3871-6 [17664457.001]
  • [Cites] J Pediatr Hematol Oncol. 2007 Sep;29(9):646-8 [17805043.001]
  • [Cites] Biochim Biophys Acta. 1998 Oct 1;1400(1-3):233-55 [9748598.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13176-81 [9789061.001]
  • [Cites] J Clin Oncol. 1998 Dec;16(12):3880-9 [9850034.001]
  • [Cites] Bone Marrow Transplant. 1999 Jan;23(1):21-5 [10037046.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):569-77 [10080601.001]
  • [Cites] Pediatr Hematol Oncol. 1999 May-Jun;16(3):267-70 [10326227.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2128-36 [17673902.001]
  • [Cites] Haematologica. 2007 Oct;92(10):1389-98 [17768113.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:453-9 [18024664.001]
  • [Cites] J Clin Oncol. 2008 Mar 1;26(7):1106-11 [18309945.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [Cites] Med Pediatr Oncol. 1989;17(6):477-84 [2586362.001]
  • [Cites] Leukemia. 1999 Mar;13(3):335-42 [10086723.001]
  • [Cites] Leukemia. 2000 Feb;14(2):232-7 [10673738.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1588-93 [10688812.001]
  • [Cites] J Clin Oncol. 2000 Mar;18(5):947-55 [10694543.001]
  • [Cites] Br J Haematol. 2000 Apr;109(1):13-23 [10848777.001]
  • [Cites] Br J Cancer. 2000 Jul;83(1):91-4 [10883674.001]
  • [Cites] J Clin Oncol. 2000 Aug;18(15):2836-42 [10920131.001]
  • [Cites] Ann Oncol. 2000 Oct;11(10):1289-94 [11106118.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2196-204 [11187911.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2205-22 [11187912.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2234-9 [11187914.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2240-6 [11187915.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2257-66 [11187917.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2267-75 [11187918.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2276-85 [11187919.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2295-306 [11187921.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2307-20 [11187922.001]
  • [Cites] Br J Haematol. 2001 Jan;112(1):109-17 [11225603.001]
  • [Cites] Med Pediatr Oncol. 2001 May;36(5):525-35 [11340607.001]
  • [Cites] Med Pediatr Oncol. 2001 May;36(5):536-40 [11340608.001]
  • [Cites] Leukemia. 2001 Jun;15(6):963-70 [11417484.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11592-7 [11553769.001]
  • [Cites] Lancet Oncol. 2001 Jul;2(7):429-36 [11905737.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Blood. 2002 Jul 15;100(2):427-34 [12091332.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1972-6 [12200354.001]
  • [Cites] Pharmacogenetics. 2002 Nov;12(8):605-11 [12439220.001]
  • [Cites] J Clin Oncol. 2003 Mar 15;21(6):1074-81 [12637473.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1195-204 [12663705.001]
  • [Cites] Blood. 2003 May 15;101(10):3862-7 [12531808.001]
  • [Cites] J Clin Oncol. 2003 Jun 1;21(11):2123-37 [12775738.001]
  • [Cites] Leukemia. 2004 Jan;18(1):120-5 [14586477.001]
  • [Cites] Clin Cancer Res. 2004 Apr 15;10(8):2675-80 [15102670.001]
  • [Cites] Int J Hematol. 2004 Apr;79(3):229-34 [15168589.001]
  • [Cites] J Clin Oncol. 2004 Jun 15;22(12):2510-1 [15197216.001]
  • [Cites] Blood. 2004 Aug 1;104(3):822-8 [15090454.001]
  • [Cites] Leukemia. 2004 Oct;18(10):1581-6 [15356657.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] J Clin Oncol. 1985 Apr;3(4):532-8 [2984346.001]
  • [Cites] Blood. 1987 Nov;70(5):1412-7 [2822173.001]
  • [Cites] Cancer. 1988 Oct 1;62(7):1364-70 [3046737.001]
  • [Cites] N Engl J Med. 1989 Jul 20;321(3):136-42 [2787477.001]
  • [Cites] J Clin Oncol. 1991 Mar;9(3):432-7 [1999712.001]
  • [Cites] N Engl J Med. 1991 Dec 12;325(24):1682-7 [1944468.001]
  • [Cites] J Clin Oncol. 1992 Jan;10(1):156-63 [1309379.001]
  • [Cites] J Clin Oncol. 1993 Feb;11(2):209-17 [8426196.001]
  • [Cites] J Clin Oncol. 1993 Jun;11(6):1039-45 [8388919.001]
  • [Cites] Leukemia. 1993 Dec;7(12):1975-86 [8255096.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1680-4 [7564509.001]
  • [Cites] Leukemia. 1996 Jan;10(1):27-31 [8558933.001]
  • (PMID = 19072983.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / P30 CA021765-31
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] L36H50F353 / Podophyllotoxin
  • [Number-of-references] 99
  • [Other-IDs] NLM/ NIHMS135594; NLM/ PMC2767267
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5. Metzgeroth G, Walz C, Score J, Siebert R, Schnittger S, Haferlach C, Popp H, Haferlach T, Erben P, Mix J, Müller MC, Beneke H, Müller L, Del Valle F, Aulitzky WE, Wittkowsky G, Schmitz N, Schulte C, Müller-Hermelink K, Hodges E, Whittaker SJ, Diecker F, Döhner H, Schuld P, Hehlmann R, Hochhaus A, Cross NC, Reiter A: Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma. Leukemia; 2007 Jun;21(6):1183-8
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  • [Title] Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma.
  • The FIP1L1-PDGFRA fusion gene has been described in patients with eosinophilia-associated myeloproliferative disorders (Eos-MPD).
  • Here, we report on seven FIP1L1-PDGFRA-positive patients who presented with acute myeloid leukemia (AML, n=5) or lymphoblastic T-cell non-Hodgkin-lymphoma (n=2) in conjunction with AML or Eos-MPD.
  • Patients were treated with imatinib (100 mg, n=5; 400 mg, n=2) either as monotherapy (n=2), as maintenance treatment after intensive chemotherapy (n=3) or in overt relapse 43 and 72 months, respectively, after primary diagnosis and treatment of FIP1L1-PDGFRA-positive disease (n=2).
  • All patients are alive, disease-free and in complete hematologic and complete molecular remission after a median time of 20 months (range, 9-36) on imatinib.
  • The median time to achievement of complete molecular remission was 6 months (range, 1-14).
  • We conclude that all eosinophilia-associated hematological malignancies should be screened for the presence of the FIP1L1-PDGFRA fusion gene as they are excellent candidates for treatment with tyrosine kinase inhibitors even if they present with an aggressive phenotype such as AML.
  • [MeSH-major] Eosinophilia / drug therapy. Leukemia, Myeloid / drug therapy. Oncogene Proteins, Fusion / analysis. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha. mRNA Cleavage and Polyadenylation Factors
  • [MeSH-minor] Acute Disease. Adult. Aged. Benzamides. Disease-Free Survival. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloproliferative Disorders / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction / methods


6. Yin CC, Abruzzo LV, Qiu X, Apostolidou E, Cortes JE, Medeiros LJ, Lu G: del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2009 Jul;192(1):18-23
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  • [Title] del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia.
  • The del(15q) chromosomal abnormality is known to occur in acute leukemias, but has rarely been described in chronic myelogenous leukemia (CML).
  • Described here are five cases of CML associated with del(15q): four men and one woman.
  • Bone marrow aspirate smears showed increased blasts in all cases at the time of del(15q) detection, in accelerated phase in two cases and myeloid blast phase in three.
  • Conventional cytogenetic analysis showed t(9;22) and del(15q), as well as other inconsistent clonal abnormalities.
  • All patients received imatinib mesylate; four received additional chemotherapy, and two had allogeneic stem cell transplantation (ASCT).
  • Of the three patients who did not receive ASCT, one died, one was in persistent blast phase, and one was in clinical remission with molecular evidence of residual disease at 16, 6, and 34 months, respectively, after identification of the del(15q).
  • Of the two patients who had ASCT, one died and one was in clinical remission with molecular evidence of disease at 15 and 64 months, respectively, after identification of the del(15q).
  • These findings indicate that del(15q) is a recurrent cytogenetic abnormality that may be seen at initial presentation of advanced disease or may emerge during disease progression.
  • Del(15q) appears to be associated with a poor prognosis in CML.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 15. Clone Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adult. Bone Marrow Cells / pathology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Chromosome Aberrations. Female. Follow-Up Studies. Gene Frequency. Humans. Karyotyping. Male. Middle Aged

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  • [Cites] Mod Pathol. 2004 Jan;17(1):96-103 [14657955.001]
  • [Cites] Cancer Genet Cytogenet. 2009 Jan 15;188(2):118-23 [19100517.001]
  • [Cites] Cancer Genet Cytogenet. 2004 Jun;151(2):146-51 [15172752.001]
  • [Cites] Am J Clin Pathol. 2004 Jun;121(6):836-42 [15198355.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):671-84, x [15271399.001]
  • [Cites] Nature. 1973 Jun 1;243(5405):290-3 [4126434.001]
  • [Cites] Cancer. 1999 Dec 15;86(12):2632-41 [10594858.001]
  • [Cites] Cancer Res. 2000 Jan 1;60(1):70-3 [10646855.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3343-56 [11071626.001]
  • [Cites] Arch Pathol Lab Med. 2001 Mar;125(3):437-9 [11231500.001]
  • [Cites] Cancer. 2002 Feb 15;94(4):1102-10 [11920481.001]
  • [Cites] Mod Pathol. 2002 Dec;15(12):1266-72 [12481006.001]
  • [Cites] Int J Cancer. 2003 Aug 10;106(1):74-7 [12794759.001]
  • [Cites] Cancer Genet Cytogenet. 2003 Jul 1;144(1):1-5 [12810248.001]
  • [Cites] Scand J Haematol. 1976 Jul;17(1):17-28 [1066809.001]
  • [Cites] Cancer. 1979 Apr;43(4):1350-7 [445335.001]
  • [Cites] Hum Genet. 1981;58(3):285-93 [6948765.001]
  • [Cites] Cancer. 1985 Feb 1;55(3):535-41 [3965107.001]
  • [Cites] Leuk Res. 1991;15(8):683-91 [1654480.001]
  • [Cites] Cancer Genet Cytogenet. 1991 Aug;55(1):35-8 [1913605.001]
  • [Cites] Leuk Lymphoma. 1993;11 Suppl 1:11-5 [8251885.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Feb;86(2):124-8 [8603337.001]
  • [Cites] Baillieres Clin Haematol. 1997 Jun;10(2):223-31 [9376661.001]
  • [Cites] Leuk Res. 1998 Sep;22(9):845-7 [9716017.001]
  • [Cites] Curr Opin Hematol. 1998 Jul;5(4):302-8 [9747637.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Am J Clin Pathol. 2005 Nov;124(5):807-14 [16203287.001]
  • [Cites] Cancer. 2006 Apr 15;106(8):1730-8 [16532439.001]
  • [Cites] J Cell Biochem. 2007 Apr 15;100(6):1376-86 [17131381.001]
  • [Cites] Cancer. 2008 May 15;112(10):2112-8 [18348294.001]
  • [Cites] Cancer. 2008 Oct 1;113(7 Suppl):1933-52 [18798533.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • (PMID = 19480932.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS627187; NLM/ PMC4167428
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7. Mainwaring MG, Rimsza LM, Chen SF, Gomez SP, Weeks FW, Reddy V, Lynch J, May WS, Kahn S, Moreb J, Leather H, Braylan R, Rowe TC, Fieniewicz KJ, Wingard JR: Treatment of refractory acute leukemia with timed sequential chemotherapy using topotecan followed by etoposide + mitoxantrone (T-EM) and correlation with topoisomerase II levels. Leuk Lymphoma; 2002 May;43(5):989-99
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  • [Title] Treatment of refractory acute leukemia with timed sequential chemotherapy using topotecan followed by etoposide + mitoxantrone (T-EM) and correlation with topoisomerase II levels.
  • A phase I/II clinical study evaluated 17 patients with refractory/recurrent acute leukemia treated with 1.5 mg/m2/day topotecan on days 1-3 followed by etoposide (100 mg/m2/day)+mitoxantrone (10 mg/m2/day) on days 4, 5 and 9, 10.
  • Timed sequential chemotherapy using the topoisomerase I-inhibitor topotecan before the topoisomerase II-inhibitors, etoposide+mitoxantrone (T-EM) treatment is proposed to induce topoisomerase II protein levels and potentiate the cytotoxic activity of the topoisomerase II-directed drugs.
  • Fourteen patients had refractory and three had recurrent acute leukemia.
  • The majority of patients were heavily pre-treated with greater than three re-induction chemotherapy regimens.
  • Ten patients responded to T-EM treatment (59%).
  • Four additional patients (24%) who scored complete leukemia clearance had no evidence of disease with complete white and red blood cell recovery but with platelet counts less than 100,000.
  • The lack of platelet recovery in one patient having a partial response was scored as a partial leukemia clearance.
  • Paired measurements of intracellular levels of topoisomerase II isoforms alpha and beta in leukemia blast cells (bone marrow) collected before (day 0) and after topotecan treatment (day 4) showed that a relative increase of topoisomerase IIalpha (Topo IIalpha) > or = 40% strongly correlated with response after T-EM treatment.
  • Two patients who had an increase of Topo IIalpha of 20-25% had either a PR or PLC while patients with a < 10% increase showed no response to T-EM treatment.
  • We conclude that timed sequential chemotherapy using topotecan followed by etoposide+mitoxantrone is an effective regimen for patients with refractory acute leukemia, and demonstrate Topo IIalpha protein level increases after topotecan treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. DNA Topoisomerases, Type II / analysis. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. DNA Fragmentation. Enzyme Induction. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Topotecan / administration & dosage

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  • (PMID = 12148910.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 7M7YKX2N15 / Topotecan; BZ114NVM5P / Mitoxantrone; EC 5.99.1.3 / DNA Topoisomerases, Type II
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8. Yanada M, Kiyoi H, Murata M, Suzuki M, Iwai M, Yokozawa T, Baba H, Emi N, Naoe T: Micafungin, a novel antifungal agent, as empirical therapy in acute leukemia patients with febrile neutropenia. Intern Med; 2006;45(5):259-64
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  • [Title] Micafungin, a novel antifungal agent, as empirical therapy in acute leukemia patients with febrile neutropenia.
  • OBJECTIVE: Invasive fungal infection is a major cause of morbidity and mortality in patients with febrile neutropenia unresponsive to antibacterial treatment.
  • Empirical antifungal therapy with amphotericin B has been the standard of care for these patients; however, there remains a need for less toxic alternative drugs.
  • PATIENTS AND METHODS: We conducted a prospective study to evaluate the efficacy and safety of micafungin (MCFG), a novel antifungal agent of the echinocandin class, in an empirical therapy setting for patients with febrile neutropenia.
  • RESULTS: A total of 31 patients with acute leukemia who developed febrile neutropenia were enrolled in the study.
  • Among them, 18 patients fulfilling the protocol-defined criteria, including 10 with persistent fever and 8 with recurrent fever, received MCFG empirically.
  • Underlying diseases consisted of acute myeloid leukemia (n=15) and acute lymphoblastic leukemia (n=3).
  • The median duration of neutropenia and drug administration was 22 and 9.5 days, respectively.
  • Treatment success, defined as defervescence during the neutropenic period, absence of breakthrough fungal infections, and requiring no replacement of antifungal drugs, was achieved in 14 patients (78%).
  • CONCLUSIONS: Although the studied patients were limited in number, our results indicate that MCFG is an encouraging agent for empirical antifungal therapy in patients with febrile neutropenia, and deserves further investigation in large-scale studies.
  • [MeSH-major] Antifungal Agents / therapeutic use. Lipoproteins / therapeutic use. Neutropenia / drug therapy. Peptides, Cyclic / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Algorithms. Echinocandins. Female. Fever / etiology. Humans. Leukemia, Myeloid / complications. Lipopeptides. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Prospective Studies

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  • (PMID = 16595990.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 0 / Lipopeptides; 0 / Lipoproteins; 0 / Peptides, Cyclic; R10H71BSWG / micafungin
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9. Sarkodee-Adoo C, Pittarelli L, Jaffe E, Sorbara L, Raffeld M, Yao X, Haddad R, Heller T: Regression and clonally distinct recurrence of human immunodeficiency virus related Burkitt-like lymphoma during antiretroviral therapy. Leuk Lymphoma; 2001 Sep-Oct;42(5):1125-31
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  • [Title] Regression and clonally distinct recurrence of human immunodeficiency virus related Burkitt-like lymphoma during antiretroviral therapy.
  • An increased incidence of intermediate to high-grade Non Hodgkin's Lymphoma is found in individuals with AIDS.
  • Although immune function in AIDS patients can be improved through the use of antiretroviral therapy, the contribution of these drugs to lymphoma regression is not known.
  • Here we describe the complete regression and subsequent recurrence of high grade, Burkitt-like lymphoma during antiretroviral therapy in a patient with AIDS.
  • Antiretroviral therapy resulted in diminished viral load and modest improvement in CD4+ T cell counts.
  • Lymphoma regressed initially, but relapsed 3 months later.
  • Tissue taken from the initial and recurrent tumor demonstrated different clonal rearrangements.
  • The recurrent lymphoma did not respond to continued antiretroviral therapy.
  • In Conclusion, antiretroviral therapy may contribute to lymphoma regression in AIDS lymphoma.
  • Clinically recurrent disease may be clonally distinct.
  • [MeSH-major] Anti-HIV Agents / administration & dosage. Lymphoma, AIDS-Related / drug therapy. Lymphoma, AIDS-Related / pathology
  • [MeSH-minor] Adult. Burkitt Lymphoma. Clone Cells / pathology. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / pathology. Male. Neoplasms, Second Primary / pathology. Recurrence. Remission Induction

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  • (PMID = 11697632.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Anti-HIV Agents
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10. Jung SI, Cho HS, Lee CH, Jung BC: A case of adult B lymphoblastic leukemia with ider(9)(q10)t(9;22)(q34;q11.2) and der(19)t(1;19)(q23;p13.3). Korean J Lab Med; 2010 Dec;30(6):585-90
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  • [Title] A case of adult B lymphoblastic leukemia with ider(9)(q10)t(9;22)(q34;q11.2) and der(19)t(1;19)(q23;p13.3).
  • In B lymphoblastic leukemia/lymphoma (B-ALL/LBL), t(9;22)(q34;q11.2) and t(1;19)(q23;p13.3) are recurrent cytogenetic abnormalities.
  • Here, we report a case of adult B-ALL with ider(9)(q10)t(9;22)(q34;q11.2) and der(19)t(1;19)(q23;p13.3).
  • A literature review revealed that ider(9) (q10)t(9;22) is a rare variant of t(9;22) with a deletion of the short arm of chromosome 9.
  • This abnormality is specific to precursor B-lymphoid neoplasms, such as B-ALL or B-lymphoid blast phase of CML, and is associated with disease progression or short survival.
  • The patient underwent imatinib therapy in addition to intensive chemotherapy, but failed to achieve remission.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Translocation, Genetic

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  • (PMID = 21157143.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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11. Wu S, Korte A, Gessner R, Henze G, Seeger K: Levels of the soluble, 55-kilodalton isoform of tumor necrosis factor receptor in bone marrow are correlated with the clinical outcome of children with acute lymphoblastic leukemia in first recurrence. Cancer; 2003 Aug 1;98(3):625-31
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  • [Title] Levels of the soluble, 55-kilodalton isoform of tumor necrosis factor receptor in bone marrow are correlated with the clinical outcome of children with acute lymphoblastic leukemia in first recurrence.
  • The objective of the current study was to determine the levels of sTNFRp55 and their impact on outcome in 106 children with acute lymphoblastic leukemia (ALL) in first recurrence.
  • METHODS: Between January 1997 and December 2001, bone marrow (BM) samples were collected from 106 children with a first recurrence of ALL at diagnosis.
  • Levels of sTNFRp55 in BM samples were determined with a commercially available enzyme-linked immunosorbent assay kit.
  • High levels of sTNFRp55 were associated with shorter duration of first complete remission and observation time as well as poor response to chemotherapy.
  • Most importantly, the probability of EFS (pEFS) at 3 years was significantly worse for children with recurrent ALL who had sTNFRp55 levels greater than the median value (> 2.77 ng/mL) compared with patients who had levels that were less than the median value (pEFS: 0.44 +/- 0.10 ng/mL vs. 0.12 +/- 0.10 ng/mL; P = 0.006).
  • It is noteworthy that the sTNFRp55 levels in 22 children with recurrent, TEL-AML1-positive ALL ([t(12;21)(p13;q22)]; 2.69 +/- 1.05 ng/mL) were significantly lower compared with the levels in children who had TEL-AML1-negative ALL (3.34 +/- 1.49 ng/mL; P < 0.05).
  • CONCLUSIONS: The results indicated that a high sTNFRp55 level represents a negative prognostic factor for children with recurrent ALL in terms of EFS and overall survival.
  • [MeSH-major] Antigens, CD / metabolism. Bone Marrow / metabolism. Neoplasm Recurrence, Local / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Tumor Necrosis Factor / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / metabolism. Child. Child, Preschool. Disease-Free Survival. Enzyme-Linked Immunosorbent Assay. Female. Humans. Infant. Male. Middle Aged. Molecular Weight. Neoplasm Staging. Protein Isoforms. Receptors, Tumor Necrosis Factor, Type I. Remission Induction. Solubility. Survival Rate

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  • [Copyright] Copyright 2003 American Cancer Society.DOI 10.1002/cncr.11553
  • (PMID = 12879482.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Protein Isoforms; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Type I
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12. Jillella AP, Day DS, Severson K, Kallab AM, Burgess R: Non-Hodgkin's lymphoma presenting as anasarca: probably mediated by tumor necrosis factor alpha (TNF-alpha). Leuk Lymphoma; 2000 Jul;38(3-4):419-22
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  • [Title] Non-Hodgkin's lymphoma presenting as anasarca: probably mediated by tumor necrosis factor alpha (TNF-alpha).
  • Both patients were treated with CHOP chemotherapy.
  • She relapsed two months later with recurrent edema that responded a second time to salvage chemotherapy.
  • The second patient died of gram positive sepsis a week after diagnosis.
  • As anasarca is an unusual presenting symptom of non-Hodgkin's lymphoma, we postulated that the malignant cells were secreting a cytokine that resulted in "vascular leakage" of fluid and development of diffuse edema.
  • [MeSH-major] Edema / etiology. Lymphoma, Large B-Cell, Diffuse / complications. Lymphoma, T-Cell / complications. Neoplasm Proteins / physiology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Capillary Leak Syndrome / etiology. Cyclophosphamide / administration & dosage. Cytokines / blood. Doxorubicin / administration & dosage. Fatal Outcome. Female. Humans. Male. Prednisone / administration & dosage. Serum Albumin / deficiency. Vincristine / administration & dosage

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  • (PMID = 10830750.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 0 / Cytokines; 0 / Neoplasm Proteins; 0 / Serum Albumin; 0 / Tumor Necrosis Factor-alpha; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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13. Robak T, Smolewski P, Cebula B, Szmigielska-Kaplon A, Chojnowski K, Blonski JZ: Rituximab combined with cladribine or with cladribine and cyclophosphamide in heavily pretreated patients with indolent lymphoproliferative disorders and mantle cell lymphoma. Cancer; 2006 Oct 1;107(7):1542-50
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  • [Title] Rituximab combined with cladribine or with cladribine and cyclophosphamide in heavily pretreated patients with indolent lymphoproliferative disorders and mantle cell lymphoma.
  • METHODS: For the current study, the authors evaluated the feasibility, efficacy, and toxicity of combined regimens that consisted of either rituximab plus cladribine (2-CdA) (the RC regimen) or RC plus cyclophosphamide (the RCC regimen) in the treatment of patients with heavily pretreated, indolent lymphoid malignancies.
  • Fifty-four adult patients with recurrent or refractory, low-grade non-Hodgkin lymphoma (LG-NHL) and B-cell chronic lymphocytic leukemia (B-CLL) were treated according to the RC/RCC regimens.
  • RESULTS: Thirty-three patients with B-CLL, 12 patients with LG-NHL and 9 patients with mantle cell lymphoma (MCL) entered the study.
  • Thirty-three patients (61%) had recurrent disease after prior therapy, and 21 patients (39%) had refractory disease.
  • The treatment revealed tolerability, with episodes of severe neutropenia (Grade 3 and 4 [according to World Health Organization criteria]) observed in 6 patients (11%), episodes of Grade 3 and 4 infections observed in 11 patients (20%), and episodes of Grade 3-4 thrombocytopenia observed in 4 patients (7%).
  • CONCLUSIONS: The RC and RCC regimens were highly effective and well tolerated modalities of treatment in heavily pretreated patients with indolent lymphoproliferative disorders.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols. Cladribine / therapeutic use. Cyclophosphamide / therapeutic use. Lymphoma, Mantle-Cell / drug therapy. Lymphoproliferative Disorders / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Murine-Derived. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Rituximab. Treatment Outcome

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 16948126.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 47M74X9YT5 / Cladribine; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide
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14. Bittencourt AL, de Oliveira Mde F: Cutaneous manifestations associated with HTLV-1 infection. Int J Dermatol; 2010 Oct;49(10):1099-110
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  • [Title] Cutaneous manifestations associated with HTLV-1 infection.
  • Skin lesions are frequent in human T-cell lymphotropic virus type 1 (HTLV-1) infection and may constitute an alert for the diagnosis of this condition.
  • The most severe skin diseases related to this virus are adult T-cell leukemia/lymphoma (ATLL), an aggressive form of leukemia/lymphoma that fails to respond to chemotherapy, and infective dermatitis associated with HTLV-1 (IDH), a severe and recurrent form of eczema occurring in childhood.
  • IDH may progress to HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and to ATLL.
  • Adult onset IDH and reactional and inflammatory dermatoses found in carriers and also in patients with HAM/TSP will be considered.
  • Other dermatological diseases that occur more frequently in HTLV-1-infected individuals such as xerosis, acquired ichthyosis, seborrheic dermatitis and infectious and parasitic dermatoses will also be discussed.
  • [MeSH-major] Lymphoma, T-Cell / pathology. Lymphoma, T-Cell / virology
  • [MeSH-minor] Antiviral Agents / therapeutic use. Carrier State. Diagnosis, Differential. Drug Resistance, Neoplasm. HTLV-I Infections. Human T-lymphotropic virus 1. Humans. Ichthyosis / diagnosis. Ichthyosis / virology. Immunohistochemistry. Interferon-alpha / therapeutic use. Scabies / diagnosis. Skin / pathology. Skin Diseases, Viral / diagnosis. Treponemal Infections / diagnosis. Zidovudine / therapeutic use

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  • [Copyright] © 2010 The International Society of Dermatology.
  • (PMID = 20883400.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 4B9XT59T7S / Zidovudine
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15. Moore S, Suttle J, Bain S, Story C, Rice M: Acute lymphoblastic leukemia characterized by t(8;14)(q11.2;q32). Cancer Genet Cytogenet; 2003 Feb;141(1):1-4
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  • [Title] Acute lymphoblastic leukemia characterized by t(8;14)(q11.2;q32).
  • The t(8;14)(q11.2;q32) is emerging as an uncommon, though recurrent cytogenetic finding.
  • As of yet, too few cases of acute lymphoblastic leukemia (ALL) characterized by this translocation have been studied to determine its prognostic significance with confidence.
  • We therefore report three new patients (two male children and one adult female) and present their hematologic, immunophenotypic, and clinical data.
  • The total number of patients now reported in the literature is 29 with a mean age of 14 years.
  • Early relapse, that is, relapse within 6 months, does not appear to be a common feature of this group.
  • Twenty-three t(8;14) patients show a pre-B immunophenotype and 24 of 24, on whom information is available, achieved complete remission after induction chemotherapy for B-ALL.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 8 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Genes, Immunoglobulin / genetics. Humans. Male. Middle Aged

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  • (PMID = 12581891.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
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16. Matsumoto Y, Nomura K, Kanda-Akano Y, Fujita Y, Nakao M, Ueda K, Horiike S, Yokota S, Kusuzaki K, Kitoh T, Watanabe A, Taniwaki M: Successful treatment with Erwinia L-asparaginase for recurrent natural killer/T cell lymphoma. Leuk Lymphoma; 2003 May;44(5):879-82
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  • [Title] Successful treatment with Erwinia L-asparaginase for recurrent natural killer/T cell lymphoma.
  • We describe a patient with natural killer (NK)/T cell lymphoma who relapsed after autologous peripheral blood stem cell transplantation (auto-PBSCT) and was successfully treated with Escherichia coli (E. coli) and Erwinia L-asparaginase.
  • A 38-year-old male patient with ulcerated tumor at the left thigh was diagnosed as having nasal type NK/T cell lymphoma on the basis of histopathological and flowcytometric findings of tumor, revealing diffuse infiltration of atypical lymphoid cells into blood vessels and expression of CD7 and CD56 antigens, but not CD3.
  • After five cycles of CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) therapy, the patient achieved complete remission and received high-dose chemotherapy with auto-PBSCT, although the tumor recurred in the right leg 10 months later.
  • Despite salvage chemotherapy, followed by local irradiation and surgical amputation, a tumor recurred at the left upper gingiva 10 days after.
  • The asparagine synthetase expression in tumor cells was immunohistochemically negative on paraffin-embedded tissues.
  • L-asparaginase is a promising agent for the treatment of NK/T cell lymphoma.
  • [MeSH-major] Asparaginase / administration & dosage. Killer Cells, Natural / pathology. Lymphoma, T-Cell / drug therapy
  • [MeSH-minor] Adult. Anaphylaxis / chemically induced. Erwinia / enzymology. Escherichia coli Proteins / adverse effects. Humans. Male. Neoplasm Invasiveness / pathology. Peripheral Blood Stem Cell Transplantation. Recurrence. Remission Induction / methods. Treatment Outcome

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  • (PMID = 12802930.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Escherichia coli Proteins; EC 3.5.1.1 / Asparaginase
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17. Han Y, Xue Y, Zhang J, Wu Y, Pan J, Wang Y, Shen J, Dai H, Bai S: Translocation (14;14)(q11;q32) with simultaneous involvement of the IGH and CEBPE genes in B-lineage acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2008 Dec;187(2):125-9
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  • [Title] Translocation (14;14)(q11;q32) with simultaneous involvement of the IGH and CEBPE genes in B-lineage acute lymphoblastic leukemia.
  • Translocation (14;14)(q11;q32) is one of the recurrent chromosome aberrations in ataxia-teleangiectasia (AT) and T-cell malignancies.
  • However, t(14;14)(q11;q32) is an exceedingly rare phenomenon in B-lineage acute lymphoblastic leukemia (B-ALL).
  • Here, we report another B-ALL case with t(14;14)(q11;q32) in a 39-year-old female.
  • Fluorescence in situ hybridization (FISH) demonstrated trisomy 4 and the simultaneous involvement of the IGH gene at 14q32 and the CEBPE gene at 14q11, which differs from the genes involved in T-cell leukemias.
  • After chemotherapy, the patient achieved complete remission (CR).
  • Later, she received allogeneic peripheral blood stem cell transplantation.
  • We suggest that t(14;14)(q11;q32) involving the IGH and CEBPE genes in B-ALL is rare, but it is a recurrent abnormality that could identify a new subgroup of B-ALL.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Chromosomes, Human, Pair 14 / genetics. Immunoglobulin Heavy Chains / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / genetics. Daunorubicin / therapeutic use. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Prednisone / therapeutic use. Trisomy. Vincristine / therapeutic use

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  • (PMID = 19027493.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CCAAT-Enhancer-Binding Proteins; 0 / Immunoglobulin Heavy Chains; 142805-41-2 / CEBPE protein, human; 5J49Q6B70F / Vincristine; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; VDP protocol
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18. Bielen D, Mortelé K, Peters H, Lombard D, Ros R: Small bowel obstruction secondary to disseminated candidiasis in an immunocompromised patient: radiologic-pathologic correlation. JBR-BTR; 2005 Jan-Feb;88(1):20-2
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  • Immunosuppression for therapeutic reasons (e.g. post transplantation, post chemotherapy), as well as pathologic immunodeficiency due to certain pathologic conditions (e.g.
  • AIDS, leukemia), is increasingly encountered in daily medical practice.
  • We report on a case of a 33-year-old immunocompromised woman with a history of recurrent T-cell lymphoblastic lymphoma, which presented with abdominal pain.
  • Computed tomography (CT) images demonstrated significant small bowel dilatation, wall thickening, and high-density intestinal content, with a focal point of transition in the pelvis.
  • [MeSH-major] Candidiasis / diagnosis. Immunocompromised Host. Intestinal Obstruction / microbiology. Jejunal Diseases / microbiology. Opportunistic Infections / diagnosis
  • [MeSH-minor] Adult. Enteritis / microbiology. Fatal Outcome. Female. Humans. Lymphoma, T-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 15792164.001).
  • [ISSN] 0302-7430
  • [Journal-full-title] JBR-BTR : organe de la Société royale belge de radiologie (SRBR) = orgaan van de Koninklijke Belgische Vereniging voor Radiologie (KBVR)
  • [ISO-abbreviation] JBR-BTR
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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19. Singhal S, Powles R, Henslee-Downey PJ, Chiang KY, Treleaven J, Godder K, Kulkarni S, van Rhee F, Sirohi B, Pinkerton CR, Meller S, Mehta J: Allogeneic transplantation from HLA-matched sibling or partially HLA-mismatched related donors for primary refractory acute leukemia. Bone Marrow Transplant; 2002 Feb;29(4):291-5
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  • [Title] Allogeneic transplantation from HLA-matched sibling or partially HLA-mismatched related donors for primary refractory acute leukemia.
  • Allogeneic transplantation is successful in a minority of patients with primary refractory acute leukemia (PRAL).
  • All MSD patients received non-T cell-depleted marrow whereas all PMRD patients received partially T cell-depleted marrow.
  • Six patients in each group with recurrent/persistent disease died.
  • Ten PMRD (3-year probability 70%) and 14 MSD (3-year probability 63%) patients died of treatment-related causes.
  • We conclude that allogeneic transplantation is a viable therapeutic option for PRAL.
  • In terms of identifying a donor and harvesting cells, a PMRD transplant is significantly quicker than an unrelated donor transplant - a point of great practical importance in the setting of failed induction chemotherapy where time is of the essence.
  • [MeSH-major] HLA Antigens. Hematopoietic Stem Cell Transplantation. Leukemia / immunology. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child. Child, Preschool. Female. Graft vs Host Disease / etiology. Histocompatibility Testing. Humans. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Living Donors. Male. Middle Aged. Nuclear Family. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Retrospective Studies. Transplantation, Homologous

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  • (PMID = 11896425.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA Antigens
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20. Kalil N, Cheson BD: Management of chronic lymphocytic leukaemia. Drugs Aging; 2000 Jan;16(1):9-27
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  • [Title] Management of chronic lymphocytic leukaemia.
  • Chronic lymphocytic leukaemia (CLL) is the most common form of adult leukaemia in Western countries.
  • The diagnosis requires mature-appearing lymphocytes in the peripheral blood to >5 x 10(9)/L.
  • The immunophenotype typically includes B cell antigens CD19, CD20 and CD23, low expression of surface immunoglobulin and CD5+, with other T cell antigens absent.
  • Bone marrow biopsy, although not required for diagnosis, must show at least 30% lymphocytes.
  • Cytogenetic abnormalities are frequent in patients with CLL, and may be associated with poor prognosis.
  • Aggressive transformation occurs in 10% of patients with CLL, most commonly prolymphocytic leukaemia (PLL) and Richter's syndrome.
  • PLL de novo must be differentiated from PLL of an aggressive transformation.
  • The current recommendation to start treatment includes disease-related symptoms, massive and/or progressive hepatosplenomegaly or lymphadenopathy, increasing bone marrow failure, autoimmune disease, and recurrent infections.
  • Fludarabine is the drug of choice for the majority of patients with CLL.
  • No drug combination is better than single agents.
  • For patients refractory to initial treatment, referral to a clinical trial is the best choice.
  • Other salvage therapy includes retreatment with the same initial agent (chlorambucil or fludarabine) if initial response was observed, or fludarabine for patients refractory to chlorambucil.
  • Promising new approaches include cycle-active agents, nelarabine, biological therapy such as anti-CD52 monoclonal antibody, bone marrow transplantation, including the use of submyeloablative preparative regimens ('minitransplant') to induce graft-versus-leukaemia effect, and gene therapy.
  • Assessment of response to therapy in CLL has been updated by the National Cancer Institute Working Group, and these guidelines are used worldwide for clinical trials.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Animals. Combined Modality Therapy. Humans. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic / therapy

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  • [Cites] J Natl Cancer Inst. 1978 Aug;61(2):337-40 [277720.001]
  • [Cites] N Engl J Med. 1998 May 21;338(21):1506-14 [9593789.001]
  • [Cites] CA Cancer J Clin. 1998 Jan-Feb;48(1):6-29 [9449931.001]
  • [Cites] Semin Hematol. 1987 Oct;24(4):252-6 [3686047.001]
  • [Cites] Blood. 1984 Sep;64(3):642-8 [6466871.001]
  • [Cites] J Clin Oncol. 1999 May;17(5):1574-9 [10334546.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1885-9 [9586905.001]
  • [Cites] Am J Hematol. 1988 Nov;29(3):152-63 [3189311.001]
  • [Cites] Cancer. 1987 Dec 1;60(11):2712-6 [3677006.001]
  • [Cites] J Natl Cancer Inst. 1992 Sep 16;84(18):1422-7 [1512794.001]
  • [Cites] J Clin Oncol. 1993 Apr;11(4):671-8 [8097527.001]
  • [Cites] Br J Cancer. 1990 Jul;62(1):4-5 [2390480.001]
  • [Cites] Eur J Haematol. 1991 Apr;46(4):202-4 [2015875.001]
  • [Cites] Tumori. 1982 Dec 31;68(6):511-4 [6820205.001]
  • [Cites] Exp Hematol. 1993 Jan;21(1):61-5 [8093352.001]
  • [Cites] Br J Haematol. 1995 Mar;89(3):627-9 [7734364.001]
  • [Cites] Cancer. 1984 Aug 15;54(4):697-701 [6589030.001]
  • [Cites] Cancer. 1981 Dec 1;48(11):2447-57 [7296493.001]
  • [Cites] Blood. 1988 Dec;72(6):1884-90 [3264192.001]
  • [Cites] Blood. 1993 Jun 1;81(11):2878-84 [8499626.001]
  • [Cites] Blood. 1989 May 1;73(6):1426-30 [2713486.001]
  • [Cites] Leukemia. 1988 Mar;2(3):157-64 [3347094.001]
  • [Cites] Leuk Lymphoma. 1991;5 Suppl 1:89-91 [27463486.001]
  • [Cites] Br J Haematol. 1989 Jun;72(2):141-9 [2757960.001]
  • [Cites] Hematol Oncol. 1988 Jan-Mar;6(1):7-12 [3277904.001]
  • [Cites] Eur J Haematol. 1997 Aug;59(2):82-8 [9293855.001]
  • [Cites] N Engl J Med. 1988 Oct 6;319(14 ):902-7 [2901668.001]
  • [Cites] Nouv Rev Fr Hematol. 1988;30(5-6):457-9 [2464793.001]
  • [Cites] Ann Hematol. 1998 Mar-Apr;76(3-4):101-10 [9619726.001]
  • [Cites] Nouv Rev Fr Hematol. 1988;30(5-6):359-61 [3222145.001]
  • [Cites] Leukemia. 1995 Sep;9(9):1444-9 [7658710.001]
  • [Cites] J Biol Response Mod. 1988 Feb;7(1):97-113 [3373237.001]
  • [Cites] Blood. 1991 Sep 15;78(6):1545-51 [1884021.001]
  • [Cites] Cancer Res. 1986 Nov;46(11):5953-8 [2428488.001]
  • [Cites] Am J Hematol. 1981;10(1):9-18 [6973272.001]
  • [Cites] Leukemia. 1997 Apr;11 Suppl 2:S38-41 [9178837.001]
  • [Cites] Am J Clin Pathol. 1990 Mar;93(3):333-9 [1689938.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1631-5 [9324281.001]
  • [Cites] Br J Haematol. 1986 May;63(1):93-104 [2939873.001]
  • [Cites] Blood. 1982 Nov;60(5):1110-21 [6751436.001]
  • [Cites] J Biol Response Mod. 1985 Jun;4(3):310-23 [3874930.001]
  • [Cites] Neth J Med. 1985;28(3):112-8 [3982571.001]
  • [Cites] Bone Marrow Transplant. 1997 Apr;19(7):647-51 [9156240.001]
  • [Cites] J Clin Oncol. 1995 Apr;13(4):983-8 [7707127.001]
  • [Cites] Br J Haematol. 1973 Aug;25(2):171-7 [4726900.001]
  • [Cites] J Mol Med (Berl). 1999 Feb;77(2):266-81 [10023780.001]
  • [Cites] J Clin Oncol. 1984 Aug;2(8):881-91 [6379121.001]
  • [Cites] J Clin Oncol. 1998 Jul;16(7):2313-20 [9667245.001]
  • [Cites] Am J Med. 1991 Feb;90(2):223-8 [1996592.001]
  • [Cites] N Engl J Med. 1993 Mar 18;328(11):812-3 [8094889.001]
  • [Cites] Oncologist. 1999;4(5):352-69 [10551552.001]
  • [Cites] Semin Hematol. 1998 Jul;35(3 Suppl 3):14-21 [9685175.001]
  • [Cites] J Clin Oncol. 1995 Mar;13(3):570-4 [7884417.001]
  • [Cites] J Clin Oncol. 1998 Jan;16(1):56-62 [9440723.001]
  • [Cites] J Clin Oncol. 1998 Nov;16(11):3607-15 [9817282.001]
  • [Cites] Am J Med. 1985 Feb;78(2):216-20 [3970047.001]
  • [Cites] J Clin Oncol. 1997 Jan;15(1):37-43 [8996122.001]
  • [Cites] J Clin Oncol. 1985 Sep;3(9):1196-201 [2993534.001]
  • [Cites] Haematologica. 1990 Jan-Feb;75(1):75-8 [2338291.001]
  • [Cites] J Clin Oncol. 1997 Jul;15(7):2667-72 [9215839.001]
  • [Cites] Leukemia. 1995 Jul;9(7):1130-5 [7630184.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • [Cites] Blood. 1977 Dec;50(6):1049-59 [336116.001]
  • [Cites] Am J Hematol. 1997 Apr;54(4):342 [9092698.001]
  • [Cites] Acta Haematol. 1991;85(1):31-3 [2011927.001]
  • [Cites] N Engl J Med. 1993 Mar 18;328(11):812; author reply 813 [8094888.001]
  • [Cites] Nouv Rev Fr Hematol. 1988;30(5-6):429-32 [3065738.001]
  • [Cites] J Clin Oncol. 1986 Jan;4(1):74-9 [2416889.001]
  • [Cites] Cancer. 1981 Apr 1;47(7):1849-51 [6939479.001]
  • [Cites] Clin Exp Immunol. 1992 Sep;89(3):374-7 [1516254.001]
  • [Cites] Arch Intern Med. 1974 Oct;134(4):721-4 [4415396.001]
  • [Cites] Leuk Lymphoma. 1999 Jun;34(1-2):151-7 [10350343.001]
  • [Cites] Blood. 1987 Mar;69(3):929-36 [3814821.001]
  • [Cites] Cancer. 1981 Jul 1;48(1):198-206 [7237385.001]
  • [Cites] JAMA. 1975 Apr 21;232(3):267-9 [47401.001]
  • [Cites] Cancer. 1981 Jul 1;48(1):48-57 [7237391.001]
  • [Cites] Br J Haematol. 1987 Jan;65(1):23-9 [3468997.001]
  • [Cites] Cancer. 1994 Mar 1;73(5):1425-32 [8111709.001]
  • [Cites] Am J Hematol. 1995 Jun;49(2):135-42 [7771465.001]
  • [Cites] Leukemia. 1991 Feb;5(2):150-5 [1673487.001]
  • [Cites] J Clin Oncol. 1993 Oct;11(10):1985-9 [8410123.001]
  • [Cites] Blood. 1990 Apr 1;75(7):1414-21 [2180492.001]
  • [Cites] N Engl J Med. 1993 Mar 18;328(11):813-4 [8094890.001]
  • [Cites] Am J Hematol. 1987 Oct;26(2):179-89 [3116843.001]
  • [Cites] Leuk Lymphoma. 1997 Jun;26(1-2):83-8 [9250791.001]
  • [Cites] Ann Hematol. 1991 Jul;63(1):1-4 [1715191.001]
  • [Cites] Eur J Haematol. 1997 Jan;58(1):46-50 [9020373.001]
  • [Cites] Cancer. 1984 Sep 15;54(6):978-80 [6590113.001]
  • [Cites] Leuk Lymphoma. 1996 May;21(5-6):467-72 [9172812.001]
  • [Cites] Cancer Treat Rep. 1986 Sep;70(9):1117-20 [3488805.001]
  • [Cites] Am J Med. 1990 Sep;89(3):388-90 [1697447.001]
  • [Cites] Cancer. 1990 Jul 15;66(2):246-50 [2369709.001]
  • [Cites] Cancer. 1973 Mar;31(3):502-8 [4693581.001]
  • [Cites] Blood. 1989 May 1;73(6):1431-9 [2713487.001]
  • [Cites] Cancer. 1995 Mar 1;75(5):1104-8 [7850708.001]
  • [Cites] Leuk Lymphoma. 1996 Aug;22(5-6):509-14 [8882965.001]
  • [Cites] J Natl Cancer Inst. 1993 Apr 21;85(8):658-62 [8468724.001]
  • [Cites] Am J Hematol. 1992 Sep;41(1):5-12 [1503099.001]
  • [Cites] Br J Haematol. 1997 May;97(2):466-73 [9163617.001]
  • [Cites] Lancet. 1990 Sep 29;336(8718):820 [1698237.001]
  • [Cites] Blood. 1992 Feb 1;79(3):576-85 [1370636.001]
  • [Cites] Br J Haematol. 1986 Jun;63(2):377-87 [3487341.001]
  • [Cites] Oncology. 1985;42(6):350-3 [4069549.001]
  • [Cites] N Engl J Med. 1990 Apr 19;322(16):1117-21 [1969613.001]
  • [Cites] Am J Hematol. 1992 Aug;40(4):264-9 [1354412.001]
  • [Cites] Blood. 1990 Apr 1;75(7):1422-5 [2180493.001]
  • [Cites] Hematol Cell Ther. 1996 Aug;38(4):359-60 [8891729.001]
  • [Cites] Recenti Prog Med. 1986 Feb;77(2):100-3 [3715170.001]
  • [Cites] Blood. 1996 Dec 1;88(11):4259-64 [8943862.001]
  • [Cites] J Clin Oncol. 1995 Sep;13(9):2431-48 [7666104.001]
  • [Cites] Br J Haematol. 1986 Mar;62(3):567-75 [3954968.001]
  • [Cites] Clin Lab Haematol. 1988;10(4):391-5 [3250787.001]
  • [Cites] Leuk Lymphoma. 1991;5 Suppl 1:101-3 [27463489.001]
  • [Cites] J Clin Oncol. 1991 Sep;9(9):1562-9 [1714949.001]
  • [Cites] J Clin Oncol. 1989 Apr;7(4):433-8 [2784491.001]
  • [Cites] Br J Haematol. 1989 Nov;73(3):334-40 [2690923.001]
  • [Cites] Blood. 1997 Sep 15;90(6):2188-95 [9310469.001]
  • [Cites] Blood. 1981 Mar;57(3):406-17 [6970050.001]
  • [Cites] Ann Intern Med. 1998 Oct 1;129(7):559-66 [9758577.001]
  • [Cites] Am J Hematol. 1985 May;19(1):63-73 [3845763.001]
  • [Cites] Blood. 1989 Nov 1;74(6):2070-5 [2478221.001]
  • [Cites] Bone Marrow Transplant. 1994 Feb;13(2):217-9 [8205094.001]
  • [Cites] Br J Haematol. 1986 Nov;64(3):469-78 [3466642.001]
  • [Cites] J Natl Cancer Inst. 1990 Sep 5;82(17):1416-20 [2388293.001]
  • [Cites] N Engl J Med. 1991 Jul 11;325(2):81-6 [1904989.001]
  • [Cites] Blood. 1999 Mar 1;93(5):1732-7 [10029603.001]
  • [Cites] Ann Oncol. 1998 Sep;9(9):1023-6 [9818078.001]
  • [Cites] Am J Hematol. 1992 Sep;41(1):45-9 [1503098.001]
  • [Cites] J Clin Pathol. 1986 Jul;39(7):713-6 [3488334.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2454-60 [10561309.001]
  • [Cites] Leuk Lymphoma. 1993;10 Suppl:139-45 [8097653.001]
  • [Cites] Blood. 1988 May;71(5):1295-8 [3258768.001]
  • [Cites] Ann Intern Med. 1992 Sep 15;117(6):466-9 [1354425.001]
  • [Cites] Br J Cancer. 1991 Jul;64(1):120-3 [1713049.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] N Engl J Med. 1992 Oct 8;327(15):1056-61 [1355853.001]
  • [Cites] Hematol Oncol. 1991 Nov-Dec;9(6):315-21 [1748398.001]
  • [Cites] Br J Haematol. 1990 Sep;76(1):45-57 [2223648.001]
  • [Cites] Blood. 1989 Jul;74(1):19-25 [2473795.001]
  • [Cites] Br J Haematol. 1997 Mar;96(3):617-9 [9054672.001]
  • [Cites] Blood. 1975 Aug;46(2):219-34 [1139039.001]
  • [Cites] Cancer. 1987 Dec 1;60(11):2637-40 [3677002.001]
  • [Cites] Eur J Haematol. 1997 Aug;59(2):124-5 [9293862.001]
  • [Cites] J Clin Oncol. 1996 Jul;14(7):2160-6 [8683250.001]
  • [Cites] J Clin Oncol. 1994 Oct;12(10):2216-28 [7931492.001]
  • [Cites] Cancer. 1985 Nov 15;56(10):2369-75 [3899346.001]
  • [Cites] Semin Oncol. 1998 Feb;25(1):98-106 [9482531.001]
  • [Cites] J Clin Pathol. 1989 Jun;42(6):567-84 [2738163.001]
  • [Cites] Cancer. 1982 Apr 15;49(8):1524-9 [6950800.001]
  • [Cites] Cancer. 1978 May;41(5):1664-9 [647620.001]
  • [Cites] Br J Haematol. 1987 Oct;67(2):235-9 [3499930.001]
  • [Cites] Cancer Treat Rep. 1979 Mar;63(3):441-7 [371799.001]
  • [Cites] Cancer Treat Rep. 1986 Oct;70(10):1225-8 [2428492.001]
  • [Cites] Invest New Drugs. 1987;5(2):207-10 [2443463.001]
  • [Cites] Br J Haematol. 1995 Oct;91(2):341-4 [8547072.001]
  • [Cites] Leukemia. 1998 Nov;12(11):1699-707 [9823944.001]
  • [Cites] Blood. 1999 Mar 15;93(6):1992-2002 [10068672.001]
  • [Cites] Blood. 1993 Aug 15;82(4):1366-76 [7688995.001]
  • [Cites] Haematologica. 1996 Mar-Apr;81(2):121-6 [8641639.001]
  • [Cites] Lancet. 1990 Nov 3;336(8723):1130 [1700245.001]
  • [Cites] Br J Haematol. 1979 Jul;42(3):488-90 [476003.001]
  • [Cites] Leuk Lymphoma. 1991;5 Suppl 1:93-6 [27463487.001]
  • [Cites] Cancer. 1984 Aug 1;54(3):397-9 [6587931.001]
  • [Cites] J Clin Oncol. 1997 Jan;15(1):52-60 [8996124.001]
  • [Cites] Eur J Haematol. 1992 May;48(5):266-70 [1644158.001]
  • [Cites] Br J Haematol. 1986 Sep;64(1):77-86 [3463362.001]
  • [Cites] Bone Marrow Transplant. 1998 Mar;21(6):627-8 [9580345.001]
  • [Cites] J Clin Oncol. 1993 Apr;11(4):679-89 [8097528.001]
  • [Cites] Am J Hematol. 1987 Nov;26(3):279-84 [3674007.001]
  • [Cites] Cancer Res. 1992 Feb 15;52(4):897-903 [1737352.001]
  • [Cites] Semin Oncol. 1992 Dec;19(6):695-706 [1361080.001]
  • [Cites] J Clin Oncol. 1987 Mar;5(3):398-406 [3819805.001]
  • [Cites] Cancer Chemother Pharmacol. 1985;15(3):233-5 [2414021.001]
  • [Cites] J Clin Oncol. 1991 May;9(5):770-6 [2016618.001]
  • [Cites] J Clin Oncol. 1991 Jan;9(1):175-88 [1702143.001]
  • [Cites] Nouv Rev Fr Hematol. 1989;31(6):413-5 [2616270.001]
  • [Cites] Br J Haematol. 1991 Oct;79 Suppl 1:30-3 [1931705.001]
  • [Cites] Am J Hematol. 1990 Mar;33(3):189-97 [2405649.001]
  • [Cites] J Clin Oncol. 1986 Feb;4(2):128-36 [3511183.001]
  • [Cites] Nouv Rev Fr Hematol. 1988;30(5-6):433-6 [3065739.001]
  • [Cites] Leuk Lymphoma. 1991;5 Suppl 1:133-8 [27463495.001]
  • [Cites] Leuk Lymphoma. 1990;2(6):391-7 [27457043.001]
  • [Cites] Leukemia. 1999 Apr;13(4):518-23 [10214856.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3804-16 [9808574.001]
  • [Cites] J Natl Cancer Inst. 1987 Jan;78(1):91-4 [3467132.001]
  • [Cites] Eur J Haematol. 1987 Feb;38(2):123-30 [3595807.001]
  • [Cites] Br J Haematol. 1982 Apr;50(4):627-36 [6978147.001]
  • [Cites] J Clin Oncol. 1994 Apr;12(4):748-58 [8151318.001]
  • [Cites] Ann Intern Med. 1988 May;108(5):733-43 [3282467.001]
  • [Cites] Ann Intern Med. 1993 Jan 15;118(2):114-6 [8416307.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):458-65 [9053466.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1695-700 [8400226.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1981 Dec;7(12):1623-32 [7037702.001]
  • [Cites] Haematologica. 1989 Sep-Oct;74(5):481-5 [2511118.001]
  • [Cites] J Clin Invest. 1982 Dec;70(6):1148-56 [6816810.001]
  • [Cites] Leuk Lymphoma. 1993 Jun;10(3):187-93 [8220117.001]
  • [Cites] Acta Haematol. 1991;85(4):209-11 [1853684.001]
  • [Cites] Ann Intern Med. 1996 Feb 1;124(3):311-5 [8554226.001]
  • [Cites] Semin Oncol. 1998 Feb;25(1):42-59 [9482526.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2817-24 [9704734.001]
  • [Cites] Lancet. 1996 May 25;347(9013):1432-8 [8676625.001]
  • [Cites] Blood. 1998 Feb 1;91(3):756-63 [9446633.001]
  • [Cites] N Engl J Med. 1990 Sep 20;323(12):833-4 [1697401.001]
  • [Cites] Eur J Haematol. 1999 Feb;62(2):76-82 [10052709.001]
  • [Cites] N Engl J Med. 1994 Feb 3;330(5):319-22 [7904047.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1165-71 [9694704.001]
  • [Cites] J Clin Oncol. 1997 Apr;15(4):1567-74 [9193354.001]
  • [Cites] Ann Oncol. 1992 Feb;3(2):171-2 [1606091.001]
  • (PMID = 10733261.001).
  • [ISSN] 1170-229X
  • [Journal-full-title] Drugs & aging
  • [ISO-abbreviation] Drugs Aging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 236
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21. Janik JE, Morris JC, Pittaluga S, McDonald K, Raffeld M, Jaffe ES, Grant N, Gutierrez M, Waldmann TA, Wilson WH: Elevated serum-soluble interleukin-2 receptor levels in patients with anaplastic large cell lymphoma. Blood; 2004 Nov 15;104(10):3355-7
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  • [Title] Elevated serum-soluble interleukin-2 receptor levels in patients with anaplastic large cell lymphoma.
  • Levels of serum soluble interleukin 2 receptor (sIL-2R) provide a reliable marker of disease activity in patients with hairy cell leukemia and adult T-cell leukemia/lymphoma.
  • The malignant cells in patients with anaplastic large cell lymphoma (ALCL) express CD30 and are usually positive for expression of CD25.
  • We measured serum sIL-2R and soluble CD30 (sCD30) levels in patients with ALCL treated with EPOCH (etoposide, prednisone, Oncovin, Cytoxan, hydroxydaunorubicin) infusional chemotherapy.
  • Serum sCD30 levels were elevated and decreased in response to therapy as previously reported.
  • Serum sIL-2R levels were elevated in 7 of 9 patients with ALCL and decreased in response to treatment.
  • Patients positive for the anaplastic lymphoma kinase (ALK) gene showed elevated sIL-2R levels, whereas those negative for ALK had normal serum sIL-2R levels and their tumors lacked CD25 expression.
  • Serum sIL-2R levels were elevated in both patients with recurrent disease.
  • [MeSH-major] Biomarkers, Tumor / blood. Lymphoma, Large B-Cell, Diffuse / blood. Receptors, Interleukin-2 / blood
  • [MeSH-minor] Adult. Aged. Antigens, CD30 / blood. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Etoposide / therapeutic use. Female. Humans. Male. Middle Aged. Prednisone / therapeutic use. Recurrence. Solubility. Vincristine / therapeutic use

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  • (PMID = 15205267.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / Receptors, Interleukin-2; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; EPOCH protocol
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22. Huang CL, Lin ZZ, Su IJ, Chao TY, Tien HF, Chang MC, Huang MC, Kao WY, Tang JL, Yeh KH, Wang CH, Hsu CH, Liu MY, Cheng AL: Combination of 13-cis retinoic acid and interferon-alpha in the treatment of recurrent or refractory peripheral T-cell lymphoma. Leuk Lymphoma; 2002 Jul;43(7):1415-20
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  • [Title] Combination of 13-cis retinoic acid and interferon-alpha in the treatment of recurrent or refractory peripheral T-cell lymphoma.
  • We previously reported the therapeutic efficacy of 13-cis retinoic acid (13-cRA) in some subtypes of peripheral T-cell lymphoma (PTCL).
  • This study sought to clarify if the addition of interferon-alpha2a (IFN-alpha2a), an agent with synergistic cytotoxicity with 13-cRA in many types of malignant cells, may be more effective in the treatment of PTCL.
  • Eligible patients has histologically proven PTCL, which was recurrent after or refractory to anthracycline-containing systemic chemotherapy.
  • The treatment included oral administration of 13-cRA 1 mg/kg/day, divided into three doses, and intramuscular injection of IFN-alpha2a 4.5 MU/M2, three times per week.
  • From March 1995 to July 2000, a total of 17 patients, 10 men and 7 women, with a median age of 47 years (range, 18-77 years), were recruited.
  • The histologic diagnosis included 7 cases of unspecified PTCL, 6 cases of Ki-1 anaplastic large cell lymphoma (ALCL), 1 case of angioimmunoblastic T-cell lymphoma, and 3 cases of angiocentric nasal NK/T cell lymphoma.
  • They received a median of 1.7 months of treatment (range, 0.4-13.3 months).
  • One patient refused further treatment due to toxicity.
  • Grade III/IV hematologic and non-hematologic toxicity developed in 2 and 5 patients, respectively.
  • There were 5 partial responses (Ki-1, 4; unspecified PTCL, 1), with a total response rate of 31.3% (95% CI, 5.7-56.8%).
  • In conclusion, a combination of 13-cRA and IFN-alpha2a is a useful salvage treatment for selected patients with recurrent or refractory PTCL, particularly those with the Ki-1 subtype.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lymphoma, T-Cell, Peripheral / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Interferon-alpha / administration & dosage. Isotretinoin / administration & dosage. Male. Middle Aged. Recombinant Proteins. Remission Induction. Salvage Therapy. Survival Analysis. Survival Rate

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  • (PMID = 12389622.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 76543-88-9 / interferon alfa-2a; EH28UP18IF / Isotretinoin
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23. Robak T, Smolewski P, Urbanska-Rys H, Gora-Tybor J, Blonski JZ, Kasznicki M: Rituximab followed by cladribine in the treatment of heavily pretreated patients with indolent lymphoid malignancies. Leuk Lymphoma; 2004 May;45(5):937-44
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  • [Title] Rituximab followed by cladribine in the treatment of heavily pretreated patients with indolent lymphoid malignancies.
  • The purpose of this study was to determine the efficacy and toxicity of combined therapy consisting of rituximab (RIT), an anti-CD20 monoclonal antibody, and cladribine (2-chlorodeoxyadenosine, 2-CdA) (RC regimen) in patients with refractory or relapsed indolent lymphoproliferative disorders.
  • Twenty six CD20 antigen positive patients, 15 with B-cell chronic lymphocytic leukemia (B-CLL) and 11 with low grade non-Hodgin's lymphoma (LG-NHL) were enrolled to the study.
  • Fourteen patients (53.8%) had refractory disease, the other 12 (46.2%) were recurrent after prior chemotherapy.
  • Four patients (15.4%) (95% CI 1.5-29.3%), 1 with B-CLL and 3 with LG-NHL, achieved a complete response (CR).
  • Anemia and thrombocytopenia associated with RC treatment were observed in 5 (19.2%) and 2 patients (7.7%), respectively.
  • There was no treatment related mortality.
  • In conclusion, the combination of RIT and 2-CdA is an effective and well tolerated treatment, even for heavily pre-treated patients, and the results seem to be better than in patients previously treated in our institution with 2-CdA alone.
  • This regimen can be considered as an alternative treatment of CD-20 positive indolent lymphoproliferative disorders.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoproliferative Disorders / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antigens, CD20. Cladribine / administration & dosage. Female. Hematologic Diseases / chemically induced. Humans. Male. Middle Aged. Opportunistic Infections / chemically induced. Remission Induction / methods. Rituximab. Salvage Therapy / methods. Survival Analysis

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  • (PMID = 15291352.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 47M74X9YT5 / Cladribine; 4F4X42SYQ6 / Rituximab
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24. Ravandi F, Kantarjian H, Jones D, Dearden C, Keating M, O'Brien S: Mature T-cell leukemias. Cancer; 2005 Nov 1;104(9):1808-18
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  • [Title] Mature T-cell leukemias.
  • Mature T-cell and NK-cell leukemias are a group of relatively uncommon neoplasms derived from mature or postthymic T-cells accounting for a relatively small percentage of lymphoid malignancies.
  • The recent availability of modern immunophenotypic and molecular tools has allowed a better distinction of these disorders from their B-cell counterparts.
  • Similarly, identification of recurrent cytogenetic abnormalities, as well as plausible mechanisms through which these molecular events influence cellular signaling pathways, have created further insight into the pathogenesis of these disorders.
  • Furthermore, the availability of new agents such as alemtuzumab has generated significant interest in devising specific therapeutic strategies for these malignancies.
  • Herein, we review the clinical and pathological features of mature T-cell leukemias.
  • [MeSH-major] Leukemia, T-Cell / diagnosis
  • [MeSH-minor] Adult. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Human T-lymphotropic virus 1. Humans. Immunophenotyping. Leukemia, Lymphoid. Leukemia, Prolymphocytic / diagnosis. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic / genetics. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / virology. Middle Aged. Tumor Virus Infections

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 16136598.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 143
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25. Ishitsuka K, Utsunomiya A, Aosaki S, Tashiro Y, Takeshita T: [Indolent primary gastric adult T-cell leukemia/lymphoma with recurrent lesions limited to the stomach and duodenum]. Rinsho Ketsueki; 2002 Jul;43(7):554-9
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  • [Title] [Indolent primary gastric adult T-cell leukemia/lymphoma with recurrent lesions limited to the stomach and duodenum].
  • Biopsy specimens revealed a CD4-positive malignant lymphoma.
  • The serum anti-human T-lymphotrophic virus type I (HTLV-I) antibody test was positive.
  • He was diagnosed as having primary gastric adult T-cell leukemia/lymphoma (ATLL; acute type).
  • Complete remission was achieved with chemotherapy.
  • In December 1998, the patient experienced a relapse.
  • The lesions were limited to the region between the upper gastric body and the fornix and disappeared with radiation therapy.
  • A second relapse was detected in the gastric greater curvature and descending portion of the duodenum in May 1999 but spontaneously disappeared in 5 months.
  • The third relapse in May 2000 was systemic.
  • Monoclonal integration of the HTLV-I provirus was observed in DNA extracted from ascitic lymphocytes.
  • Chemotherapy was resumed, but the response was poor.
  • [MeSH-major] Duodenal Neoplasms / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Stomach Neoplasms / pathology

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  • (PMID = 12229125.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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26. Gondo H, Himeji D, Kamezaki K, Numata A, Tanimoto T, Takase K, Aoki K, Henzan H, Nagafuji K, Miyamoto T, Ishikawa F, Shimoda K, Inaba S, Tsukamoto H, Horiuchi T, Nakashima H, Otsuka T, Kato K, Kuroiwa M, Higuchi M, Shibuya T, Kamimura T, Kuzushima K, Tsurumi T, Kanda Y, Harada M: Reconstitution of HLA-A*2402-restricted cytomegalovirus-specific T-cells following stem cell transplantation. Int J Hematol; 2004 Dec;80(5):441-8
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  • [Title] Reconstitution of HLA-A*2402-restricted cytomegalovirus-specific T-cells following stem cell transplantation.
  • Cytomegalovirus (CMV)-specific immune reconstitution early after stem cell transplantation (SCT) was evaluated prospectively by detecting CD8+ T-cells, which recognize the peptide QYDPVAALF in the context of HLA-A*2402.
  • The numbers of CMV-specific T-cells in patients who developed grade II to IV acute graft-versus-host disease (GVHD) and received corticosteroids for acute GVHD were low in the early period after allogeneic SCT.
  • The reconstitution of CMV-specific CD8+ T-cells was delayed in patients with CMV disease or recurrent CMV reactivation.
  • These observations suggest that the detection of CMV-specific T-cells with an HLA-peptide tetramer is useful to assess immune reconstitution against CMV and to identify patients at risk for CMV disease or recurrent CMV reactivation after SCT.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Cytomegalovirus / immunology. Cytomegalovirus Infections / immunology. HLA-A Antigens / immunology. Hematopoietic Stem Cell Transplantation. Oligopeptides / immunology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Aged. Antigens, CD34 / immunology. Cell Proliferation. Female. Graft vs Host Disease / drug therapy. Graft vs Host Disease / immunology. Humans. Leukemia, Lymphoid / therapy. Leukemia, Myeloid / therapy. Lymphoma, Non-Hodgkin / therapy. Male. Middle Aged. Transplantation, Homologous


27. Elstrom RL, Martin P, Ostrow K, Barrientos J, Chadburn A, Furman R, Ruan J, Shore T, Schuster M, Cerchietti L, Melnick A, Coleman M, Leonard JP: Response to second-line therapy defines the potential for cure in patients with recurrent diffuse large B-cell lymphoma: implications for the development of novel therapeutic strategies. Clin Lymphoma Myeloma Leuk; 2010 Jun;10(3):192-6
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  • [Title] Response to second-line therapy defines the potential for cure in patients with recurrent diffuse large B-cell lymphoma: implications for the development of novel therapeutic strategies.
  • BACKGROUND: Patients with diffuse large B-cell lymphoma (DLBCL) who are not cured by initial therapy sometimes experience disease-free survival after autologous stem cell transplantation.
  • Chemotherapy responsiveness before transplantation is a major predictor of outcome.
  • Patients not responding to second-line regimens may receive third-line therapy in the hopes of achieving response, but outcome data are limited.
  • PATIENTS AND METHODS: We identified patients with relapsed or refractory DLBCL at Weill Cornell Medical Center for whom data on responses to second-line chemotherapy were available.
  • RESULTS: A total of 74 patients with relapsed or refractory DLBCL who underwent second-line chemotherapy between 1996 and 2007 were identified.
  • The choice of third-line aggressive chemotherapy instead of less intensive approaches did not confer a survival benefit.
  • CONCLUSION: Our data demonstrate that patients with recurrent DLBCL not responding to second-line chemotherapy demonstrate dismal outcomes.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / surgery. Neoplasm Recurrence, Local / surgery. Salvage Therapy / methods
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Stem Cell Transplantation. Treatment Outcome. Young Adult

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  • (PMID = 20511164.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Yamamoto K, Nagata K, Morita Y, Inagaki K, Hamaguchi H: Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10). Leuk Res; 2007 May;31(5):713-8
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  • [Title] Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10).
  • We describe here the first case of acute lymphoblastic leukemia (ALL) with an isodicentric Philadelphia [idic(Ph)] chromosome.
  • A 35-year-old man was diagnosed as ALL because of the infiltration of CD10(+)CD19(+)CD33(+)CD34(+) lymphoblasts in the bone marrow and the expression of p190-type BCR/ABL fusion transcript.
  • The idic(Ph) chromosome was spindle-shaped and supposed to be formed by two Ph chromosomes joined at their q terminals, whereas idic(Ph) chromosomes in chronic myelogenous leukemia (CML) have been shown to be fused at the satellite regions of p arms.
  • The patient did not respond to any chemotherapy and could not achieve remission.
  • Furthermore, considering other three reported cases, der(7;12)(q10;q10) may be one of the recurrent translocations in ALL.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male

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  • (PMID = 16979235.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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29. Manoukian G, Hagemeister F: Denileukin diftitox: a novel immunotoxin. Expert Opin Biol Ther; 2009 Nov;9(11):1445-51
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  • RESULTS: In 1999, the FDA approved the use of denileukin diftitox for patients with persistent or relapsed CD25-positive cutaneous T-cell lymphoma (CTCL), but Ontak has been reported to be an effective therapy for other neoplastic and non-neoplastic conditions.
  • Oncological uses include therapy for CD25-negative T-cell lymphoma, recurrent and refractory chronic lymphocytic leukemia (CLL), non-Hodgkin's B-cell lymphoma (NHL), and human T-cell lymphotropic virus- 1 (HTLV-1)-associated adult T-cell leukemia/lymphoma (ATL).
  • Potential additional uses of Ontak include: therapy of graft-versus-host disease (GvHD) and autoimmune conditions, including psoriasis, rheumatoid arthritis (RA), systemic lupus, scleroderma and vasculitis.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Diphtheria Toxin / therapeutic use. Interleukin-2 / therapeutic use. Lymphoma, T-Cell / drug therapy
  • [MeSH-minor] Humans. Recombinant Fusion Proteins / therapeutic use. United States. United States Food and Drug Administration

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  • (PMID = 19817678.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
  • [Number-of-references] 37
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30. Tarella C, Cuttica A, Vitolo U, Liberati M, Di Nicola M, Cortelazzo S, Rosato R, Rosanelli C, Di Renzo N, Musso M, Pavone E, Santini G, Pescarollo A, De Crescenzo A, Federico M, Gallamini A, Pregno P, Romano R, Coser P, Gallo E, Boccadoro M, Barbui T, Pileri A, Gianni AM, Levis A: High-dose sequential chemotherapy and peripheral blood progenitor cell autografting in patients with refractory and/or recurrent Hodgkin lymphoma: a multicenter study of the intergruppo Italiano Linfomi showing prolonged disease free survival in patients treated at first recurrence. Cancer; 2003 Jun 1;97(11):2748-59
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-dose sequential chemotherapy and peripheral blood progenitor cell autografting in patients with refractory and/or recurrent Hodgkin lymphoma: a multicenter study of the intergruppo Italiano Linfomi showing prolonged disease free survival in patients treated at first recurrence.
  • BACKGROUND: The objective of the current study was to evaluate in a multicenter setting the feasibility and efficacy of a high-dose sequential (HDS) chemotherapy regimen that combined intensive debulking and high-dose therapy (HDT) with peripheral blood progenitor cell (PBPC) autografting in patients with refractory or recurrent Hodgkin lymphoma (HL).
  • METHODS: Data were collected from 102 patients with HL who were treated with the HDS regimen at 14 centers associated with the Intergruppo Italiano Linfomi.
  • There were five toxic deaths (treatment-related mortality rate, 4.9%) and six secondary malignan cies (five patients developed myelodysplastic syndrome/acute myelogenous leukemia, and one patient developed colorectal carcinoma).
  • Patients who received HDS chemotherapy after multiple recurrences had an intermediate outcome.
  • Multivariate analysis showed that refractory disease and systemic symptoms at the time of initial presentation were associated significantly associated with poor OS and EFS.
  • CONCLUSIONS: The use of HDS chemotherapy for patients with refractory and/or recurrent HL is feasible at the multicenter level.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Hodgkin Disease / drug therapy. Hodgkin Disease / therapy
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Cyclophosphamide / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Male. Melphalan / administration & dosage. Methotrexate / administration & dosage. Middle Aged. Mitoxantrone / administration & dosage. Prognosis. Transplantation, Autologous. Treatment Outcome

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  • [Copyright] Copyright 2003 American Cancer Society.
  • (PMID = 12767087.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; Q41OR9510P / Melphalan; YL5FZ2Y5U1 / Methotrexate
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31. Kokoris SI, Siakantaris MP, Kontopidou FN, Kyrtsonis MC, Tsakris A, Spanakis N, Anargyrou K, Vassilakopoulos TP, Viniou NA, Korkolopoulou P, Dimitrakopoulou AD, Legakis N, Pangalis GA: Adult T-cell leukemia/lymphoma (ATLL): report of two fully documented Hellenic patients. Leuk Lymphoma; 2004 Apr;45(4):715-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma (ATLL): report of two fully documented Hellenic patients.
  • ATLL is etiologically associated with HTLV-I retrovirus.
  • Bone marrow biopsy revealed a normal cellularity with dyserythropoiesis and scattered small lymphocytes (CD4 + on immunostaining) Serum HTLV I and II antibodies were positive.
  • T-cell receptor gamma-chain rearrangement was positive in blood lymphocytes by PCR.
  • DNA analysis by PCR demonstrated the integration of the HTLV-I DNA in the DNA of the neoplastic T cells.
  • Both patients rapidly developed acute type ATLL.
  • Corticosteroid treatment was initiated, with gradual improvement.
  • She suffered from recurrent opportunistic infections.
  • She is currently under interferon and zidovudine therapy with stable blood parameters.
  • Chemotherapy was administered to the other patient with > 50% initial response.
  • Both patients' families were tested for serum anti HTLV-I antibodies and their mates were found to be positive; they also had detectable viral DNA by PCR analysis while asymptomatic, with no abnormal clinical findings and normal white blood cell count and morphology.
  • Investigation for HTLV-I antibodies should be mandatory in all patients with T-cell lymphoproliferative disorders.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / transmission
  • [MeSH-minor] CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / pathology. DNA, Viral / analysis. Family Health. Female. Greece. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 2 / genetics. Humans. Immunophenotyping. Male. Middle Aged. Polymerase Chain Reaction. Serologic Tests. Zidovudine / therapeutic use

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  • [ErratumIn] Leuk Lymphoma. 2004 Oct;45(10):2173-4
  • (PMID = 15160945.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral; 4B9XT59T7S / Zidovudine
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32. Fortune AF, Kelly K, Sargent J, O'Brien D, Quinn F, Chadwick N, Flynn C, Conneally E, Browne P, Crotty GM, Thornton P, Vandenberghe E: Large granular lymphocyte leukemia: natural history and response to treatment. Leuk Lymphoma; 2010 May;51(5):839-45
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  • [Title] Large granular lymphocyte leukemia: natural history and response to treatment.
  • Large granular lymphocyte leukemia (T-LGL) is an indolent T lymphoproliferative disorder that was difficult to diagnose with certainty until clonality testing of the T cell receptor gene became routinely available.
  • We studied the natural history and response to treatment in 25 consecutive patients with T-LGL diagnosed between 2004 and 2008 in which the diagnosis was confirmed by molecular analysis, to define an effective treatment algorithm.
  • The median age at diagnosis was 61 years (range 27-78), with a male to female ratio of 1:1.8 and presenting features of fatigue (n = 13), recurrent infections (n = 9), and/or abnormal blood counts (n = 5).
  • Pentostatin was the single most effective therapy, with a response rate of 75% and minimal toxicity.
  • The overall survival (OS) and progression-free survival (PFS) 37 months from diagnosis were 80% and 52%, respectively.
  • Treatment of T-LGL should be reserved for patients with symptomatic disease, but in this series, pentostatin treatment was less toxic and more effective than cyclosporine or methotrexate.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclosporine / therapeutic use. Immunosuppressive Agents / therapeutic use. Leukemia, Large Granular Lymphocytic / drug therapy
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / administration & dosage. Drug Therapy, Combination. Female. Humans. Male. Methotrexate / administration & dosage. Middle Aged. Pentostatin / administration & dosage. Survival Rate. Treatment Outcome

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  • (PMID = 20367569.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Immunosuppressive Agents; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab; 83HN0GTJ6D / Cyclosporine; YL5FZ2Y5U1 / Methotrexate
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33. Loureiro P, Southern SO, Southern PJ, Pombo-de-Oliveira MS: Clinicopathological studies of a patient with adult T-cell leukemia and pseudogynecomasty. Am J Hematol; 2000 Nov;65(3):256-9
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  • [Title] Clinicopathological studies of a patient with adult T-cell leukemia and pseudogynecomasty.
  • We present a rare case of adult T cell leukemia/lymphoma (ATL) in which leukemic T cells expressed CD4 and CD25 surface antigens and infiltrated mammary glands during clinical course of the disease.
  • The patient proved to be seropositive for human T-cell lymphotropic virus type I (HTLV-I) antibodies.
  • Monoclonal expansion of lymphoid cells integrated with HTLV-I genome was observed, and the diagnosis of ATL chronic type was made.
  • He underwent a chemotherapy regimen, and skin lesions and leukocytosis improved markedly.
  • He progressed with an indolent clinical course of ATL, when he was admitted with bilateral hyperplasia of breast, recurrent skin lesions, and leukocytosis.
  • Breast biopsy revealed bilateral gynecomasty, extensive leukemic infiltration of typical ATL cells in the mammary glands, and the presence of mammary epithelial cells productively infected with HTLV-I.
  • This is the first report describing invasion of the mammary tissue with HTLV-I-transformed T-cells and HTLV-I-associated breast disease.
  • [MeSH-major] Gynecomastia / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology

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  • (PMID = 11074545.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] UNITED STATES
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34. Tanvetyanon T, Stiff PJ: Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations. Leuk Lymphoma; 2005 Jan;46(1):151-4
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  • [Title] Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations.
  • However, to date, recurrent acute pancreatitis has never been described in association with MDS.
  • Aortitis and pericarditis were diagnosed simultaneously with MDS, refractory anemia with excess blast type 2.
  • The vasculitic syndrome responded rapidly to corticosteroids, but soon after tapering of corticosteroids, acute pancreatitis developed.
  • Multiple attempts at discontinuing the drug resulted in symptomatic flare-ups.
  • Finally, his MDS transformed into acute myeloid leukemia (AML); severe acute pancreatitis closely accompanied.
  • Induction chemotherapy and high-dose corticosteroids, however, controlled both conditions.
  • A subsequent pancreatitis attack with pseudocyst formation occurred, but again was controlled with corticosteroids, although this was followed closely by another relapse of AML.
  • All etiologies for recurrent acute pancreatitis were ruled out.
  • [MeSH-major] Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / pathology. Pancreatitis / drug therapy. Pancreatitis / pathology. Steroids / therapeutic use
  • [MeSH-minor] Abdomen / pathology. Adult. Cell Transformation, Neoplastic. Humans. Male. Recurrence. Time Factors


35. Randolph TR: Advances in acute lymphoblastic leukemia. Clin Lab Sci; 2004;17(4):235-45
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  • [Title] Advances in acute lymphoblastic leukemia.
  • DATA SYNTHESIS: Acute lymphoblastic leukemia (ALL) is a stem cell disorder characterized by an overproduction of lymphoblasts in the bone marrow that eventually spill into circulation, producing lymphocytosis.
  • As with the other acute leukemias, the most common symptoms experienced by patients include fatigue, bleeding, and recurrent infections resulting from the suppression of normal hematopoiesis in the bone marrow by the accumulating blasts.
  • ALL primarily affects children and exhibits the best response to standard chemotherapy as compared to acute myeloblastic leukemias (AML).
  • In light of early treatment successes, researchers began to investigate modifications of standard treatment regimens to accommodate variability in weight, age, and response to therapy among children with ALL.
  • Individualized treatment plans were implemented where some patients received a reduced intensity course of therapy to minimize drug toxicity while others received drug intensification to maximize response.
  • More recently, research efforts have been directed at the elucidation of leukemogenic mechanisms implicated in ALL to identify specific protein mutants that can be used to design drugs tailored to interfere with the activity of these mutant protein targets.
  • Identification of chimeric proteins produced from chromosomal translocations and gene expression profiles from microarray analyses are the primary techniques used to identify the potential therapeutic targets.
  • CONCLUSION: Several reliable prognostic indicators have been identified and are being used to improve therapeutic planning and outcome prediction in ALL patients.
  • Individualized treatment regimens have been developed based on the specific characteristics of each patient to minimize treatment related adverse events and maximize response.
  • Through the use of cytogenetic, molecular, and microarray testing, ALL classification schemes have improved and potential therapeutic targets have been identified.
  • It is anticipated that the next major advance in the treatment of ALL will involve the use of designer therapies developed to specifically interfere with particular molecular abnormalities producing the leukemogenic aberration to the normal signal transduction pathways.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adult. Child. Child, Preschool. Genes, Tumor Suppressor. Humans. Infant. Mutation. Oligonucleotide Array Sequence Analysis. Translocation, Genetic

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  • (PMID = 15559730.001).
  • [ISSN] 0894-959X
  • [Journal-full-title] Clinical laboratory science : journal of the American Society for Medical Technology
  • [ISO-abbreviation] Clin Lab Sci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 41
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